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Article ; Online: A rare KMT2A::CBL transcript in an acute monoblastic leukemia patient with an unfavorable outcome.

Yu, Jinglei / Song, Fengmei / Zhang, Mingming / Xiao, Pingnan / Feng, Jingjing / Hong, Ruimin / Hu, Yongxian / Huang, He / Wei, Guoqing

Molecular biology reports

2024 Volume 51, Issue 1, Page(s) 561

Abstract: Background: Lysine [K] methyltransferase 2A (KMT2A, previously known as MLL) gene rearrangements are common in acute leukemias of various lineages and are associated with features such as chemotherapy resistance and rapid relapse. KMT2A::CBL is a rare ... ...

Abstract	Background: Lysine [K] methyltransferase 2A (KMT2A, previously known as MLL) gene rearrangements are common in acute leukemias of various lineages and are associated with features such as chemotherapy resistance and rapid relapse. KMT2A::CBL is a rare fusion of unknown pathogenesis generated by a unique interstitial deletion of chromosome 11 that has been reported across a wide age range in both acute myeloid leukemia (AML) and acute lymphoblastic leukemia (ALL) patients. The leukemogenic effect of the KMT2A::CBL rearrangement and its association with clinical prognosis have not been well clarified. Methods and results: We report the case of a 64-year-old female who was diagnosed with acute monoblastic leukemia (M5a) and who acquired the rare KMT2A::CBL fusion. The patient received multiple cycles of therapy but did not achieve remission and eventually succumbed to severe infection and disease progression. Additionally, we characterized the predicted KMT2A-CBL protein structure in this case to reveal the underlying leukemogenic mechanisms and summarized reported cases of hematological malignancies with KMT2A::CBL fusion to investigate the correlation of gene rearrangements with clinical outcomes. Conclusions: This report provides novel insights into the leukemogenic potential of the KMT2A::CBL rearrangement and the correlation between gene rearrangements and clinical outcomes.
MeSH term(s)	Female ; Humans ; Middle Aged ; Leukemia, Monocytic, Acute/genetics ; Leukemia ; Disease Progression ; Gene Rearrangement/genetics ; Hematologic Neoplasms
Language	English
Publishing date	2024-04-21
Publishing country	Netherlands
Document type	Case Reports ; Journal Article
ZDB-ID	186544-4
ISSN	1573-4978 ; 0301-4851
ISSN (online)	1573-4978
ISSN	0301-4851
DOI	10.1007/s11033-024-09543-0
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Article ; Online: Relapsed/Refractory Peripheral T-Cell Lymphoma-Associated Hemophagocytic Lymphohistiocytosis With UNC13D and CD27 Germline Mutations.

Yang, Tingting / Chen, Rongrong / Zhang, Mingming / Jing, Ruirui / Geng, Jia / Wei, Guoqing / Luo, Yi / Xiao, Pingnan / Hong, Ruimin / Feng, Jingjing / Fu, Shan / Zhao, Houli / Cui, Jiazhen / Huang, Simao / Huang, He / Hu, Yongxian

Cell transplantation

2024 Volume 33, Page(s) 9636897231221887

Abstract: Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory disease characterized by familial and acquired forms. Here, we present the case of a 26-year-old male patient with relapsed/refractory peripheral T-cell lymphoma and concurrent HLH. ... ...

Abstract	Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory disease characterized by familial and acquired forms. Here, we present the case of a 26-year-old male patient with relapsed/refractory peripheral T-cell lymphoma and concurrent HLH. Whole-exon sequencing revealed germline mutations associated with HLH, including those in critical genes such as
MeSH term(s)	Male ; Humans ; Adult ; Germ-Line Mutation ; Lymphoma, T-Cell, Peripheral ; Lymphohistiocytosis, Hemophagocytic/complications ; Lymphohistiocytosis, Hemophagocytic/genetics ; Lymphohistiocytosis, Hemophagocytic/therapy ; Neoplasm Recurrence, Local ; Mutation ; Membrane Proteins
Chemical Substances	UNC13D protein, human ; Membrane Proteins
Language	English
Publishing date	2024-01-06
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1135816-6
ISSN	1555-3892 ; 0963-6897
ISSN (online)	1555-3892
ISSN	0963-6897
DOI	10.1177/09636897231221887
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Article ; Online: HLA Fully-Mismatched Sibling-Derived CD7 CAR-T Therapy Bridging to Haploidentical Hematopoietic Stem Cell Transplantation for Hepatosplenic γδ T-cell Lymphoma.

Xu, Xueer / Zu, Cheng / Zhang, Mingming / Xiao, Pingnan / Hong, Ruimin / Feng, Jingjing / Xu, Huijun / Cui, Jiazhen / Yu, Jian / Shi, Jimin / Wei, Guoqing / Chang, Alex H / Huang, He / Hu, Yongxian

Cell transplantation

2023 Volume 32, Page(s) 9636897231194265

Abstract: While chimeric antigen receptor (CAR)-T-cell therapy has demonstrated remarkable effectiveness in the treatment of B-cell lymphomas and leukemias, research on T-cell malignancies is still limited. Here, we reported a patient with hepatosplenic γδ T-cell ... ...

Abstract	While chimeric antigen receptor (CAR)-T-cell therapy has demonstrated remarkable effectiveness in the treatment of B-cell lymphomas and leukemias, research on T-cell malignancies is still limited. Here, we reported a patient with hepatosplenic γδ T-cell lymphoma refractory to multiple lines of chemotherapy, who eventually achieved first complete remission with flow cytometry-confirmed minimal residual disease negativity after human leukocyte antigen (HLA) fully-mismatched sibling-derived CD7 CAR-T therapy. However, given the allogeneic nature, CAR-T cells dropped rapidly after a peak of 83.4% of circulating T-cells. Cytokine release syndrome, cytopenia, and infections occurred but were manageable after treatments. After the consolidative haploidentical hematopoietic stem cell transplantation (HSCT), the patient remained in remission at the end of the follow-up (13 months post-CAR-T infusion). This is the first case of relapsed/refractory hepatosplenic γδ T-cell lymphoma who achieved lasting CR after HLA fully-mismatched sibling-derived CD7 CAR-T therapy bridging to haploidentical HSCT.
MeSH term(s)	Humans ; Receptors, Chimeric Antigen ; Siblings ; Hematopoietic Stem Cell Transplantation ; Immunotherapy, Adoptive ; HLA Antigens ; Lymphoma, T-Cell
Chemical Substances	Receptors, Chimeric Antigen ; HLA Antigens
Language	English
Publishing date	2023-09-04
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1135816-6
ISSN	1555-3892 ; 0963-6897
ISSN (online)	1555-3892
ISSN	0963-6897
DOI	10.1177/09636897231194265
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Article ; Online: Skin mesenchymal niches maintain and protect AML-initiating stem cells.

Sandhow, Lakshmi / Cai, Huan / Leonard, Elory / Xiao, Pingnan / Tomaipitinca, Luana / Månsson, Alma / Kondo, Makoto / Sun, Xiaoyan / Johansson, Anne-Sofie / Tryggvason, Karl / Kasper, Maria / Järås, Marcus / Qian, Hong

The Journal of experimental medicine

2023 Volume 220, Issue 10

Abstract: Leukemia cutis or leukemic cell infiltration in skin is one of the common extramedullary manifestations of acute myeloid leukemia (AML) and signifies a poorer prognosis. However, its pathogenesis and maintenance remain understudied. Here, we report ... ...

Abstract	Leukemia cutis or leukemic cell infiltration in skin is one of the common extramedullary manifestations of acute myeloid leukemia (AML) and signifies a poorer prognosis. However, its pathogenesis and maintenance remain understudied. Here, we report massive AML cell infiltration in the skin in a transplantation-induced MLL-AF9 AML mouse model. These AML cells could regenerate AML after transplantation. Prospective niche characterization revealed that skin harbored mesenchymal progenitor cells (MPCs) with a similar phenotype as BM mesenchymal stem cells. These skin MPCs protected AML-initiating stem cells (LSCs) from chemotherapy in vitro partially via mitochondrial transfer. Furthermore, Lama4 deletion in skin MPCs promoted AML LSC proliferation and chemoresistance. Importantly, more chemoresistant AML LSCs appeared to be retained in Lama4-/- mouse skin after cytarabine treatment. Our study reveals the characteristics and previously unrecognized roles of skin mesenchymal niches in maintaining and protecting AML LSCs during chemotherapy, meriting future exploration of their impact on AML relapse.
MeSH term(s)	Animals ; Mice ; Prospective Studies ; Stem Cells ; Skin ; Leukemia, Myeloid, Acute ; Mesenchymal Stem Cells
Language	English
Publishing date	2023-07-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20220953
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Article ; Online: Progression of progenitor B-cell leukemia is associated with alterations of the bone marrow micro-environment.

Åhsberg, Josefine / Xiao, Pingnan / Okuyama, Kazuki / Somasundaram, Rajesh / Strid, Tobias / Qian, Hong / Sigvardsson, Mikael

Haematologica

2019 Volume 105, Issue 3, Page(s) e102–e106

MeSH term(s)	Bone Marrow ; Bone Marrow Cells ; Humans ; Leukemia ; Leukemia, Lymphocytic, Chronic, B-Cell ; Precursor Cells, B-Lymphoid ; Tumor Microenvironment
Language	English
Publishing date	2019-07-11
Publishing country	Italy
Document type	Letter
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2018.214031
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Article ; Online: Sequential CD7 CAR T-Cell Therapy and Allogeneic HSCT without GVHD Prophylaxis.

Hu, Yongxian / Zhang, Mingming / Yang, Tingting / Mo, Zhuomao / Wei, Guoqing / Jing, Ruirui / Zhao, Houli / Chen, Rongrong / Zu, Cheng / Gu, Tianning / Xiao, Pingnan / Hong, Ruimin / Feng, Jingjing / Fu, Shan / Kong, Delin / Xu, Huijun / Cui, Jiazhen / Huang, Simao / Liang, Bin /

Yuan, Xiaolin / Cui, Qu / Guo, Hongshan / Yu, Yunxian / Feng, Youqin / Jin, Chunxiang / Ren, Jiangtao / Chang, Alex H / Wang, Dongrui / Huang, He

The New England journal of medicine

2024 Volume 390, Issue 16, Page(s) 1467–1480

Abstract: Background: Patients with relapsed or refractory hematologic cancers have a poor prognosis. Chimeric antigen receptor (CAR) T-cell therapy as a bridge to allogeneic hematopoietic stem-cell transplantation (HSCT) has the potential for long-term tumor ... ...

Abstract	Background: Patients with relapsed or refractory hematologic cancers have a poor prognosis. Chimeric antigen receptor (CAR) T-cell therapy as a bridge to allogeneic hematopoietic stem-cell transplantation (HSCT) has the potential for long-term tumor elimination. However, pre-HSCT myeloablation and graft-versus-host disease (GVHD) prophylaxis agents have toxic effects and could eradicate residual CAR T cells and compromise antitumor effects. Whether the integration of CAR T-cell therapy and allogeneic HSCT can preserve CAR T-cell function and improve tumor control is unclear. Methods: We tested a novel "all-in-one" strategy consisting of sequential CD7 CAR T-cell therapy and haploidentical HSCT in 10 patients with relapsed or refractory CD7-positive leukemia or lymphoma. After CAR T-cell therapy led to complete remission with incomplete hematologic recovery, patients received haploidentical HSCT without pharmacologic myeloablation or GVHD prophylaxis drugs. Toxic effects and efficacy were closely monitored. Results: After CAR T-cell therapy, all 10 patients had complete remission with incomplete hematologic recovery and grade 4 pancytopenia. After haploidentical HSCT, 1 patient died on day 13 of septic shock and encephalitis, 8 patients had full donor chimerism, and 1 patient had autologous hematopoiesis. Three patients had grade 2 HSCT-associated acute GVHD. The median follow-up was 15.1 months (range, 3.1 to 24.0) after CAR T-cell therapy. Six patients remained in minimal residual disease-negative complete remission, 2 had a relapse of CD7-negative leukemia, and 1 died of septic shock at 3.7 months. The estimated 1-year overall survival was 68% (95% confidence interval [CI], 43 to 100), and the estimated 1-year disease-free survival was 54% (95% CI, 29 to 100). Conclusions: Our findings suggest that sequential CD7 CAR T-cell therapy and haploidentical HSCT is safe and effective, with remission and serious but reversible adverse events. This strategy offers a feasible approach for patients with CD7-positive tumors who are ineligible for conventional allogeneic HSCT. (Funded by the National Natural Science Foundation of China and the Key Project of Science and Technology Department of Zhejiang Province; ClinicalTrials.gov numbers, NCT04599556 and NCT04538599.).
MeSH term(s)	Humans ; Hematopoietic Stem Cell Transplantation/adverse effects ; Graft vs Host Disease/prevention & control ; Male ; Adult ; Female ; Immunotherapy, Adoptive/adverse effects ; Middle Aged ; Antigens, CD7 ; Receptors, Chimeric Antigen/therapeutic use ; Young Adult ; Combined Modality Therapy ; Leukemia/therapy ; Leukemia/mortality ; Lymphoma/therapy ; Remission Induction ; Transplantation, Homologous ; Adolescent
Chemical Substances	Antigens, CD7 ; Receptors, Chimeric Antigen
Language	English
Publishing date	2024-04-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMoa2313812
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Article ; Online: Critical role of Lama4 for hematopoiesis regeneration and acute myeloid leukemia progression.

Cai, Huan / Kondo, Makoto / Sandhow, Lakshmi / Xiao, Pingnan / Johansson, Anne-Sofie / Sasaki, Takako / Zawacka-Pankau, Joanna / Tryggvason, Karl / Ungerstedt, Johanna / Walfridsson, Julian / Ekblom, Marja / Qian, Hong

Blood

2021 Volume 139, Issue 20, Page(s) 3040–3057

Abstract: Impairment of normal hematopoiesis and leukemia progression are 2 well-linked processes during leukemia development and are controlled by the bone marrow (BM) niche. Extracellular matrix proteins, including laminin, are important BM niche components. ... ...

Abstract	Impairment of normal hematopoiesis and leukemia progression are 2 well-linked processes during leukemia development and are controlled by the bone marrow (BM) niche. Extracellular matrix proteins, including laminin, are important BM niche components. However, their role in hematopoiesis regeneration and leukemia is unknown. Laminin α4 (Lama4), a major receptor-binding chain of several laminins, is altered in BM niches in mice with acute myeloid leukemia (AML). So far, the impact of Lama4 on leukemia progression remains unknown. We here report that Lama4 deletion in mice resulted in impaired hematopoiesis regeneration following irradiation-induced stress, which is accompanied by altered BM niche composition and inflammation. Importantly, in a transplantation-induced MLL-AF9 AML mouse model, we demonstrate accelerated AML progression and relapse in Lama4-/- mice. Upon AML exposure, Lama4-/- mesenchymal stem cells (MSCs) exhibited dramatic molecular alterations, including upregulation of inflammatory cytokines that favor AML growth. Lama4-/- MSCs displayed increased antioxidant activities and promoted AML stem cell proliferation and chemoresistance to cytarabine, which was accompanied by increased mitochondrial transfer from the MSCs to AML cells and reduced reactive oxygen species in AML cells in vitro. Similarly, we detected lower levels of reactive oxygen species in AML cells from Lama4-/- mice post-cytarabine treatment. Notably, LAMA4 inhibition or knockdown in human MSCs promoted human AML cell proliferation and chemoprotection. Together, our study for the first time demonstrates the critical role of Lama4 in impeding AML progression and chemoresistance. Targeting Lama4 signaling pathways may offer potential new therapeutic options for AML.
MeSH term(s)	Animals ; Cytarabine/therapeutic use ; Drug Resistance, Neoplasm ; Hematopoiesis/genetics ; Humans ; Laminin/genetics ; Leukemia, Myeloid, Acute/drug therapy ; Mesenchymal Stem Cells ; Mice ; Mice, Knockout ; Reactive Oxygen Species
Chemical Substances	Lama4 protein, mouse ; Laminin ; Reactive Oxygen Species ; Cytarabine (04079A1RDZ)
Language	English
Publishing date	2021-12-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021011510
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Article ; Online: Characterization of the bone marrow niche in patients with chronic myeloid leukemia identifies CXCL14 as a new therapeutic option.

Dolinska, Monika / Cai, Huan / Månsson, Alma / Shen, Jingyi / Xiao, Pingnan / Bouderlique, Thibault / Li, Xidan / Leonard, Elory / Chang, Marcus / Gao, Yuchen / Medina, Juan Pablo / Kondo, Makoto / Sandhow, Lakshmi / Johansson, Anne-Sofie / Deneberg, Stefan / Söderlund, Stina / Jädersten, Martin / Ungerstedt, Johanna / Tobiasson, Magnus /

Östman, Arne / Mustjoki, Satu / Stenke, Leif / Le Blanc, Katarina / Hellström-Lindberg, Eva / Lehmann, Sören / Ekblom, Marja / Olsson-Strömberg, Ulla / Sigvardsson, Mikael / Qian, Hong

Blood

2023 Volume 142, Issue 1, Page(s) 73–89

Abstract: Although tyrosine kinase inhibitors (TKIs) are effective in treating chronic myeloid leukemia (CML), they often fail to eradicate the leukemia-initiating stem cells (LSCs), causing disease persistence and relapse. Evidence indicates that LSC persistence ... ...

Abstract	Although tyrosine kinase inhibitors (TKIs) are effective in treating chronic myeloid leukemia (CML), they often fail to eradicate the leukemia-initiating stem cells (LSCs), causing disease persistence and relapse. Evidence indicates that LSC persistence may be because of bone marrow (BM) niche protection; however, little is known about the underlying mechanisms. Herein, we molecularly and functionally characterize BM niches in patients with CML at diagnosis and reveal the altered niche composition and function in these patients. Long-term culture initiating cell assay showed that the mesenchymal stem cells from patients with CML displayed an enhanced supporting capacity for normal and CML BM CD34+CD38- cells. Molecularly, RNA sequencing detected dysregulated cytokine and growth factor expression in the BM cellular niches of patients with CML. Among them, CXCL14 was lost in the BM cellular niches in contrast to its expression in healthy BM. Restoring CXCL14 significantly inhibited CML LSC maintenance and enhanced their response to imatinib in vitro, and CML engraftment in vivo in NSG-SGM3 mice. Importantly, CXCL14 treatment dramatically inhibited CML engraftment in patient-derived xenografted NSG-SGM3 mice, even to a greater degree than imatinib, and this inhibition persisted in patients with suboptimal TKI response. Mechanistically, CXCL14 upregulated inflammatory cytokine signaling but downregulated mTOR signaling and oxidative phosphorylation in CML LSCs. Together, we have discovered a suppressive role of CXCL14 in CML LSC growth. CXCL14 might offer a treatment option targeting CML LSCs.
MeSH term(s)	Animals ; Mice ; Bone Marrow/metabolism ; Chemokines, CXC/metabolism ; Chemokines, CXC/pharmacology ; Chemokines, CXC/therapeutic use ; Cytokines/metabolism ; Imatinib Mesylate/pharmacology ; Imatinib Mesylate/therapeutic use ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/drug therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/metabolism ; Neoplastic Stem Cells/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Signal Transduction
Chemical Substances	Chemokines, CXC ; CXCL14 protein, mouse ; Cytokines ; Imatinib Mesylate (8A1O1M485B) ; Protein Kinase Inhibitors ; CXCL14 protein, human
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2022016896
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Article ; Online: Distinct roles of mesenchymal stem and progenitor cells during the development of acute myeloid leukemia in mice.

Xiao, Pingnan / Sandhow, Lakshmi / Heshmati, Yaser / Kondo, Makoto / Bouderlique, Thibault / Dolinska, Monika / Johansson, Anne-Sofie / Sigvardsson, Mikael / Ekblom, Marja / Walfridsson, Julian / Qian, Hong

Blood advances

2018 Volume 2, Issue 12, Page(s) 1480–1494

Abstract: Despite increasing evidence for the involvement of bone marrow (BM) hematopoietic stem cell niche in leukemogenesis, how BM mesenchymal stem and progenitor cells (MSPCs) contribute to leukemia niche formation and progression remains unclear. Using an MLL- ...

Abstract	Despite increasing evidence for the involvement of bone marrow (BM) hematopoietic stem cell niche in leukemogenesis, how BM mesenchymal stem and progenitor cells (MSPCs) contribute to leukemia niche formation and progression remains unclear. Using an MLL-AF9 acute myeloid leukemia (AML) mouse model, we demonstrate dynamic alterations of BM cellular niche components, including MSPCs and endothelial cells during AML development and its association with AML engraftment. Primary patient AML cells also induced similar niche alterations in xenografted mice. AML cell infiltration in BM causes an expansion of early B-cell factor 2
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors ; Bone Marrow/pathology ; Carcinogenesis/pathology ; Leukemia, Myeloid, Acute/pathology ; Mesenchymal Stem Cells/pathology ; Mice ; Myeloid-Lymphoid Leukemia Protein ; Oncogene Proteins, Fusion ; Stem Cell Niche/genetics ; Transplantation, Heterologous ; Tumor Burden ; Tumor Microenvironment
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Ebf2 protein, mouse ; MLL-AF9 fusion protein, human ; Oncogene Proteins, Fusion ; Myeloid-Lymphoid Leukemia Protein (149025-06-9)
Language	English
Publishing date	2018-06-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2876449-3
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2017013870
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Article: Nonadherent culture method downregulates stem cell antigen-1 expression in mouse bone marrow mesenchymal stem cells.

Deng, Baoping / Deng, Weiping / Xiao, Pingnan / Zeng, Kuan / Zhang, Shining / Zhang, Hongwu / Deng, David Yb / Yang, Yanqi

Experimental and therapeutic medicine

2015 Volume 10, Issue 1, Page(s) 31–36

Abstract: Mesenchymal stem cells (MSCs) are primarily isolated by their adherence to plastic and ... ...

Abstract	Mesenchymal stem cells (MSCs) are primarily isolated by their adherence to plastic and their
Language	English
Publishing date	2015-04-29
Publishing country	Greece
Document type	Journal Article
ZDB-ID	2683844-8
ISSN	1792-1015 ; 1792-0981
ISSN (online)	1792-1015
ISSN	1792-0981
DOI	10.3892/etm.2015.2457
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